Why some HIV patients remain symptom free for years without treatmentAugust 13th, 2008 - 2:54 pm ICT by ANI
Washington, August 13 (ANI): AIDS experts at Johns Hopkins say that it is probably because of the strength of the immune system, and not any defects an HIV strain, that some people infected with the virus can remain symptom free for years even without treatment.
The researchers said that this compelling evidence comes from rigorous blood and genetic studies from a monogamous, married, African-American couple in Baltimore, in which the wife was infected through sex with her husband more than a decade ago.
Revealing their findings in the Journal of Virology, the researchers revealed that the wife remains symptom free, has consistently had viral counts of fewer than 50 copies per cubic millilitre of blood, and has not needed any treatment to keep the disease in check.
The husband, on the other hand, takes a potent drug cocktail to keep his infection from developing into full-blown AIDS, as demonstrated by viral counts in the hundreds of thousands per cubic millilitre of blood.
The couple has been married for two decades, and the husband was an intravenous drug user.
The case study, insist the researchers, disproves the involvement of a defective or “weakened” viral strain in elite suppression.
“This is an extremely rare case of co-infection in a controlled, monogamous relationship, which showed us how a strong immune system in the elite suppressor kept the virus from replicating and infecting other cells,” says Dr. Joel Blankson, senior study investigator and infectious disease specialist.
“Our findings offer hope to vaccine researchers because they reveal that the immune system’’s primary offense, known as CD8 killer T-cells, can effectively halt disease progression by a pathogenic form of HIV,” says Blankson, an assistant professor at the Johns Hopkins University School of Medicine.
“Moreover, the strength of the immune response was not dependent on infection by a weakened form of the virus. And if we can harness the means by which these elite white blood cells stop the virus, then we can hopefully ”teach” or reprogram white blood cells in others to also target HIV,” he adds.
Through genetic testing, the researchers discovered that both husband and wife were infected with the same pathogenic strain of HIV, and that there were not deficiencies in the virus that infected the wife.
Genetic testing also confirmed that both husband and wife had an overactive strand of genetic material tied to gene HLA B57, found in previous studies to be more common in those whose HIV infection was suppressed or slowed.
“The presence of this genetic spot is a discordant result that strongly contradicts theories that various genetic factors alone play a protective role in suppression,” says Dr. Blankson.
The researchers also used lab tests to precisely measure the immune response to various strains of HIV, and found that activated T-cells from the wife stalled HIV replication by as much as 90 percent, while the husband’’s T-cells stopped it by only 30 percent.
Subsequent genetic analyses revealed that the viral strain in the wife’’s blood had at least two mutations known to weaken the virus, while the viral strain in the husband’’s blood had fewer mutations affecting fitness.
Blankson says that the stronger immune system in elite suppression not only lowers the viral count in the body, but also exerts selective, evolutionary pressure on the original strain of HIV to mutate away from the strong version that initially infected the couple, and towards weaker, less-fit forms.
“Elite suppression offers clues to vaccine researchers on many fronts: how CD8 killer T-cells can attack HIV and how a stronger immune response can force HIV into a permanent defensive state,” the researcher says.
Based on their observations, the researchers came to the conclusion that a new approach is needed to tackle HIV, and that it may be based on T-cell action.
He also plans to study differences in CD8 T-cells in elite suppressors and progressors, with the goal of retooling and activating T-cell action in progressors to act more like those in elite suppressors. (ANI)
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